Trillions of cells in your body perform countless vital functions, from metabolizing nutrients to producing and distributing hormones. But each cell is subject to damage and wear and tear over time – intrinsic or extrinsic aging. Researchers are increasingly exploring how comprehensive lifestyle changes may influence telomeres length and human health and disease. Blackburn and her colleagues are no exception.
The relationship between telomeres and aging is captivating yet surprisingly intricate. One consistent pattern in human research is that chronic stress, particularly the kind associated with long-term illness or unrelenting sadness and depression, can be a significant contributor to shorter leukocyte telomeres. Maltreatment, severe neglect, and exposure to violence also seem to cut a significant swath through the telomeres.
Using cross-sectional and longitudinal data, researchers have found that higher levels of self-perceived stress correlate with shorter telomeres and more oxidative damage in the blood. They estimate that the most stressed individuals experience 9-17 years of accelerated cell aging.
This is likely due to the complex interplay of glucocorticoid effects, mitochondrial oxidative damage, and inflammation that underlie short telomeres. Researchers are investigating the possibility that a longitudinal lifestyle stress buffer counteracts some of these adverse effects. For example, work by an assistant professor at UCSF suggests that moderate and intense exercise might reduce the relationship between stress and leukocyte telomere length in young adults.
Telomeres are protective caps located at the ends of our chromosomes. With each cell division, the telomeres become slightly shorter. Once they reach a certain length, the cell stops dividing or dies, called cellular senescence or biological aging.
To avoid this shortening, our bodies have an enzyme called telomerase that adds small sequences of the DNA repeat TAG to the ends of each strand of chromosomes each time the cell divides. However, this enzyme is only active in certain types of cells, including germ cells (which produce sperm and eggs) and some adult stem cells. Cells with no telomerase quickly become senescent and die, causing us to age more rapidly.
Fortunately, research suggests that exercise can increase telomerase activity and telomere length. A study published in 2021 found that endurance exercises such as brisk walking and running and resistance exercises such as weight training can keep telomeres longer and delay cellular senescence.
Numerous studies have investigated the correlation between inadequate sleep quality and telomere length. However, due to the correlational research design of these studies, causality cannot be inferred.
In one study, researchers found that individuals with a late chronotype tend to fall asleep later in the evening. The Wolves among us had significantly shorter telomeres over six years than those with an early chronotype.
It’s important to consider that the experiment conducted in the study lacked control, and the sample size was small, which may limit the reliability of the findings. For this reason, it’s essential to conduct further research with prospective designs, adequate sampling timeframes, and matched controls to ensure the results are valid and generalizable to a larger population.
Moreover, it would be beneficial to test psychological sleep interventions against telomere measurement, as this would allow us to understand whether improving sleep quality could slow cellular aging. It would require a more comprehensive study with a larger sample size, which would provide more accurate and reliable results.